Regional and temporal differential regulation of the N-methyl-D-aspartate receptor by phencyclidine during development

dc.contributor.advisor

Kenneth M. Johnson, PhD.

en_US

dc.creator

Noelle Catherine Anastasio

en_US

dc.date.accessioned

2011-12-20T16:04:59Z

dc.date.available

2008-06-17

en_US

dc.date.available

2011-12-20T16:04:59Z

dc.date.created

2005-07-20

en_US

dc.date.issued

2005-07-06

en_US

dc.identifier.other

etd-07202005-145246

en_US

dc.identifier.uri

http://hdl.handle.net/2152.3/170

dc.description.abstract

Disruptions in glutamatergic neurotransmission may play a role in the pathogenesis of schizophrenia. The purpose of this study was to determine phencyclidine (PCP)-induced changes in the NMDA receptor subunit composition and the relationship of these changes to the deficits in pre-pulse inhibition (PPI) caused by PCP treatment. Postnatal rats were treated with atypical or typical antipsychotics or selective dopamine or serotonin receptor antagonists prior to acute or sub-chronic PCP. This study provides evidence that two distinct mechanisms underlie effects of acute and sub-chronic PCP on NMDA receptor subunit up-regulation. Furthermore, we discovered that D1, D2, and 5-HT2A receptors play a pivotal role in sub-chronic PCP-induced up-regulation of NR1 and NR2A. Finally, we were able to correlate changes in NMDA receptor subunits to the behavioral effects of PCP in this animal model of schizophrenia.